Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon

Due to their large scale and uniquely branched architecture, neurons critically rely on active transport of mitochondria in order to match energy production and calcium buffering to local demand. Consequently, defective mitochondrial trafficking is implicated in various neurological and neurodegener...

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Main Authors: Tom Venneman, Pieter Vanden Berghe
Format: Article
Language:English
Published: Frontiers Media S.A. 2024-12-01
Series:Frontiers in Cellular Neuroscience
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Online Access:https://www.frontiersin.org/articles/10.3389/fncel.2024.1509283/full
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author Tom Venneman
Pieter Vanden Berghe
author_facet Tom Venneman
Pieter Vanden Berghe
author_sort Tom Venneman
collection DOAJ
description Due to their large scale and uniquely branched architecture, neurons critically rely on active transport of mitochondria in order to match energy production and calcium buffering to local demand. Consequently, defective mitochondrial trafficking is implicated in various neurological and neurodegenerative diseases. A key signal regulating mitochondrial transport is intracellular calcium. Elevated Ca2+ levels have been demonstrated to inhibit mitochondrial transport in many cell types, including neurons. However, it is currently unclear to what extent calcium-signaling regulates axonal mitochondrial transport during realistic neuronal activity patterns. We created a robust pipeline to quantify with high spatial resolution, absolute Ca2+ concentrations. This allows us to monitor Ca2+ dynamics with pixel precision in the axon and other neuronal compartments. We found that axonal calcium levels scale with firing frequency in the range of 0.1–1 μM, whereas KCl-induced depolarization generated levels almost a magnitude higher. As expected, prolonged KCl-induced depolarization did inhibit axonal mitochondrial transport in primary hippocampal neurons. However, physiologically relevant neuronal activity patterns only inhibited mitochondrial transport in axonal segments which made connections to a target neuron. In “non-connecting” axonal segments, we were unable to trigger this inhibitory mechanism using realistic firing patterns. Thus, we confirm that neuronal activity can indeed regulate axonal mitochondrial transport, and reveal a spatial pattern to this regulation which went previously undetected. Together, these findings indicate a potent, but localized role for activity-related calcium fluctuations in the regulation of axonal mitochondrial transport.
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spelling doaj-art-d910b0c14117458d9691c2f79900dfa22024-12-04T04:23:15ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022024-12-011810.3389/fncel.2024.15092831509283Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axonTom VennemanPieter Vanden BergheDue to their large scale and uniquely branched architecture, neurons critically rely on active transport of mitochondria in order to match energy production and calcium buffering to local demand. Consequently, defective mitochondrial trafficking is implicated in various neurological and neurodegenerative diseases. A key signal regulating mitochondrial transport is intracellular calcium. Elevated Ca2+ levels have been demonstrated to inhibit mitochondrial transport in many cell types, including neurons. However, it is currently unclear to what extent calcium-signaling regulates axonal mitochondrial transport during realistic neuronal activity patterns. We created a robust pipeline to quantify with high spatial resolution, absolute Ca2+ concentrations. This allows us to monitor Ca2+ dynamics with pixel precision in the axon and other neuronal compartments. We found that axonal calcium levels scale with firing frequency in the range of 0.1–1 μM, whereas KCl-induced depolarization generated levels almost a magnitude higher. As expected, prolonged KCl-induced depolarization did inhibit axonal mitochondrial transport in primary hippocampal neurons. However, physiologically relevant neuronal activity patterns only inhibited mitochondrial transport in axonal segments which made connections to a target neuron. In “non-connecting” axonal segments, we were unable to trigger this inhibitory mechanism using realistic firing patterns. Thus, we confirm that neuronal activity can indeed regulate axonal mitochondrial transport, and reveal a spatial pattern to this regulation which went previously undetected. Together, these findings indicate a potent, but localized role for activity-related calcium fluctuations in the regulation of axonal mitochondrial transport.https://www.frontiersin.org/articles/10.3389/fncel.2024.1509283/fullaxonal mitochondrial transportneuronal activityratiometric calcium imagingsynaptic connectionstransport regulation
spellingShingle Tom Venneman
Pieter Vanden Berghe
Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon
Frontiers in Cellular Neuroscience
axonal mitochondrial transport
neuronal activity
ratiometric calcium imaging
synaptic connections
transport regulation
title Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon
title_full Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon
title_fullStr Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon
title_full_unstemmed Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon
title_short Neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon
title_sort neuronal activity inhibits mitochondrial transport only in synaptically connected segments of the axon
topic axonal mitochondrial transport
neuronal activity
ratiometric calcium imaging
synaptic connections
transport regulation
url https://www.frontiersin.org/articles/10.3389/fncel.2024.1509283/full
work_keys_str_mv AT tomvenneman neuronalactivityinhibitsmitochondrialtransportonlyinsynapticallyconnectedsegmentsoftheaxon
AT pietervandenberghe neuronalactivityinhibitsmitochondrialtransportonlyinsynapticallyconnectedsegmentsoftheaxon